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RAB33A, member RAS oncogene family

Rab33A
The protein encoded by this gene belongs to the small GTPase superfamily, Rab family. It is GTP-binding protein and may be involved in vesicle transport. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Rab5, ATG16L1, Rab33B, Rab3A, HAD
Papers on Rab33A
The small GTPase Rab33A participates in regulation of amylase release from parotid acinar cells.
New
Fukuda et al., Niigata, Japan. In Biochem Biophys Res Commun, Jul 2015
Here, we studied isoproterenol (IPR)-induced amylase release from parotid acinar cells to investigate the possible involvement of Rab33A, which was recently suggested to regulate exocytosis in hippocampal neurons and PC12 cells.
Effect of non-tuberculous Mycobacteria on host biomarkers potentially relevant for tuberculosis management.
TB Trials Study Group et al., Bergen, Norway. In Plos Negl Trop Dis, 2014
The study shows a down-regulation of RAB33A (p<0.001) and up-regulation of TGFβ1, IL-2 and IL-6 (all p<0.05) in children with TB disease, and that RAB33A, TGFBR2 and IL-10 (all p<0.05) were differentially expressed in children with NTM present when compared to children that were culture negative for MTB and NTM (controls).
Analysis of 52 Rab GTPases from channel catfish and their involvement in immune responses after bacterial infections.
Liu et al., Auburn, United States. In Dev Comp Immunol, 2014
These included Rab3a, Rab4a, Rab4b, Rab5a, Rab5c, Rab7a, Rab9a, Rab11a, Rab11b, and Rab33a.
X-linked congenital ptosis and associated intellectual disability, short stature, microcephaly, cleft palate, digital and genital abnormalities define novel Xq25q26 duplication syndrome.
Kleefstra et al., Denmark. In Hum Genet, 2014
Comparison of the gene content of the individual duplications with the respective phenotypes suggested three critical regions with candidate genes (AIFM1, RAB33A, GPC3 and IGSF1) for the common phenotypes, including candidate loci for congenital bilateral ptosis, small head circumference, short stature, genital and digital defects.
Identification of biomarkers for Mycobacterium tuberculosis infection and disease in BCG-vaccinated young children in Southern India.
TB Trials Study Group et al., Bergen, Norway. In Genes Immun, 2013
The study shows that transcription of SEC14L1, GUSB, BPI, CCR7 and TGFβ-1 (all P ≤ 0.05) was downregulated in TB disease compared with uninfected controls, while transcription of RAB33A was downregulated in TB disease compared with both latent TB (P < 0.05) and controls (P < 0.01).
Expression of DNMTs and genomic DNA methylation in gastric signet ring cell carcinoma.
Wang et al., Chongqing, China. In Mol Med Report, 2013
However, MeDIP‑qPCR analysis demonstrated that specific tumor‑related genes, including ABL2, FGF18, TRAF2, EGFL7 and RAB33A were aberrantly hypomethylated in SRC tissue.
Rab33a mediates anterograde vesicular transport for membrane exocytosis and axon outgrowth.
Inagaki et al., Ikoma, Japan. In J Neurosci, 2012
Here, we show that Rab33a expression became upregulated during axon outgrowth of cultured rat hippocampal neurons.
Atg16L1, an essential factor for canonical autophagy, participates in hormone secretion from PC12 cells independently of autophagic activity.
Fukuda et al., Sendai, Japan. In Mol Biol Cell, 2012
We also find that Atg16L1 interacts with the small GTPase Rab33A and that this interaction is required for the dense-core vesicle localization of Atg16L1 in PC12 cells.
A genome-wide RNAi screen identifies novel targets of neratinib resistance leading to identification of potential drug resistant genetic markers.
Ryan et al., Cambridge, United States. In Mol Biosyst, 2012
RAB33A, RAB6A and BCL2L14), transcription factors (e.g.
Release of TNF-α from macrophages is mediated by small GTPase Rab37.
Tsuboi et al., Nagasaki, Japan. In Eur J Immunol, 2011
Rab3B, Rab27B, Rab30, Rab33A, Rab37, and Rab40C) being upregulated during the inflammation and proliferation/migration phase of skin repair.
Procathepsin L secretion, which triggers tumour progression, is regulated by Rab4a in human melanoma cells.
Frade et al., Rouen, France. In Biochem J, 2011
Rab3A, Rab4A, Rab4B, Rab5A, Rab8A, Rab11A, Rab27A and Rab33A, which are involved in distinct regulatory pathways.
Alport syndrome. Molecular genetic aspects.
Hertz, Århus, Denmark. In Dan Med Bull, 2009
One larger rearrangement was found, an inversion of 21 Mb with a proximal breakpoint in COL4A5 intron 8 at Xq22.3, and a distal breakpoint in the RAB33A gene at Xq26.1.
The expression of 16 genes related to the cell of origin and immune response predicts survival in elderly patients with diffuse large B-cell lymphoma treated with CHOP and rituximab.
Groupe d'Etude des Lymphomes de l'Adulte et al., Paris, France. In Leukemia, 2008
A multivariate model comprising four genes of the cell-of-origin signature (LMO2, MME, LPP and FOXP1) and two genes related to immune response, identified for their differential effects in R-CHOP patients (APOBEC3G and RAB33A), demonstrated a high predictive efficiency in this set of patients, suggesting that both features affect outcome in DLBCL patients receiving immunochemotherapy.
Direct link between Atg protein and small GTPase Rab: Atg16L functions as a potential Rab33 effector in mammals.
Itoh et al., Sendai, Japan. In Autophagy, 2008
We recently reported finding that Atg16L specifically and directly interacts with the Golgi-resident small GTPase Rab33B (and Rab33A) via the coiled-coil domain of Atg16L.
Golgi-resident small GTPase Rab33B interacts with Atg16L and modulates autophagosome formation.
Fukuda et al., Sendai, Japan. In Mol Biol Cell, 2008
In this study, we showed that Golgi-resident small GTPase Rab33B (and Rab33A) specifically interacts with Atg16L, an essential factor in isolation membrane formation, in a guanosine triphosphate-dependent manner.
Ras-associated small GTPase 33A, a novel T cell factor, is down-regulated in patients with tuberculosis.
GeneRIF
Kaufmann et al., Berlin, Germany. In J Infect Dis, 2005
expression was down-regulated in patients with TB and was predominantly expressed in CD8+ T cells.
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